We have studied the pathophysiology of gastrointestinal dysfunction in patients with diabetes mellitus in the past, with methods which were available up to 1967. We now propose to continue these studies for 2 reasons: the recent development of new methods for studying gastrointestinal function in man and the opportunity to participate in a multidisciplinary approach to diabetes mellitus, facilitated by a Program Project Grant (Director; Ronald K. Kalkhoff, M.D.). The following studies will be performed on patients with gastrointestinal dysfunction: 1) Gastric emptying. Hypothesis: decreased gastric emptying in response to hyperosmolality, acidity, fatty acids and L-tryptophane may be selectively accentuated by impairment of adrenergic innervation while emptying of water and saline may be normal. Duodenal and proximal jejunal receptors will be stimulated by duodenal perfusions and t1/2 of gastric emptying measured. 2) Lipolysis. Hypothesis: Gallbladder and pancreatic responses to endogenous and/or exogenous CCK may be impaired. Studies: quantitative determinations of duodenal bile acid, bilirubin and enzyme appearance with appropriate stimuli. Distribution of lipolytic products in gut contents. Bile acid pool and recycling rate. 3) Ileal dysfunction. Hypothesis: altered intestinal flow velocity, possible ileal bacterial overgrowth. Slow marker perfusion of jejunum and ileum with bacterial cultures from ileum and search for hydroxylated fatty acids.